What are drugs like Ozempic doing to the brains of people that binge eat?

Medications like Ozempic are not going anywhere anytime soon.

Twelve percent of US adults have taken a GLP-1 agonist—an increasingly popular type of prescription drug for obesity and diabetes management, that includes popular brands like Ozempic and Mounjaro.

Australia’s Therapeutic Goods Administration recently approved the type 2 diabetes drug tirzepatide (sold as Mounjaro) for use in treating obesity, leading to a nationwide shortage.

Tirzepatide and other GLP-1 agonists mimic hormones that are naturally released after eating, which help to regulate blood sugar and signal fullness to the brain.

While this explains part of their effect, researchers still don’t fully understand how they change eating habits and lead to significant weight loss in most individuals that take them.

Some people report that their intrusive thoughts around food—commonly referred to as “food noise” on social media—have disappeared when they started taking these drugs.

Although there isn’t much empirical evidence for this, these reports have led scientists to hypothesize that these medications act beyond the gut, and target circuits in the brain that control how we process rewards and seek out relief for our cravings.

Making sense of binge eating disorder

Binge eating disorder (BED) is the most prevalent eating disorder in Australia.

Those affected with binge eating disorder consume excessive amounts of food rapidly, often eating past fullness and into physical discomfort. Feelings of guilt and shame follow, further entrenching this destructive cycle and making binge eating disorder more difficult to treat.

Binge eating disorder is strongly associated with weight gain and obesity, though not all individuals with obesity have BED. Research indicates that BED is more prevalent among individuals with obesity, and it often co-occurs with other medical conditions like type 2 diabetes and cardiovascular disease.

The causes of binge eating disorder remain uncertain, but evidence suggests it is driven by compulsive neural mechanisms—the same brain pathways that regulate habit formation and addiction.

Ideally, GLP-1 medications could help people living with binge eating disorder (BED) to break this cycle by reducing their overwhelming intrusive thoughts around eating and empowering them to normalize their relationship with food.

GLP-1 agonists are not currently indicated for the treatment of binge eating disorder (BED).

Although there is some very early evidence suggesting that these medications might help reduce the frequency or intensity of binge eating episodes, no large-scale clinical trials have been completed to confirm their safety or effectiveness for this condition.

This is why GLP-1s cannot be routinely prescribed for BED and why more research is needed before they can be considered a viable treatment option.

However, these medications can also cause people to skip meals and to feel less in touch with their own natural hunger cues, a particularly troubling concern for those living with an eating disorder.

An overemphasis on weight and shape may arise in some people as they begin to experience changes to their body shape and weight.

Similarly, those in recovery may struggle to face the uncomfortable feelings that binging helped them to cope with, including past traumas and experiences of fatphobia.

For these reasons, I am wary of these drugs being seen as a cure for binge eating disorder; although they may eventually prove to be effective at reducing the frequency of binge eating episodes, I do not believe a medication should be perceived as a substitute for psychotherapy.

Perhaps the greatest cause for concern is not what happens to people with binge eating disorder when they start taking the GLP-1 medications, but rather, what happens if they stop.

People who stop taking drugs like Ozempic are known to regain the weight they lost while on the drug and it is still unknown how people with BED’s mood or compulsions to binge eat may shift if they stop using of these medications.

One month’s dose of tirzepatide can cost over AU$700 with a private prescription, meaning that people with limited economic resources may not be able to afford the long-term use of a drug they benefit from.

Economic precarity and food insecurity have both been found to be risk factors for binge eating disorder, meaning that those who could stand to benefit the most from potential new interventions may not be able to afford them.

A new study led by my team at the University of Melbourne aims to test the theory that these drugs can break the cycle of binge eating by tracking how GLP-1 drugs change the brains of people living with BED.

For this study, adults with BED will complete an MRI scan right before they begin taking a GLP-1 medication and after taking the drug for six months.

The issues above, among many others, have led us to incorporate several precautionary measures into our study design. For example, all participants with BED will also receive regular support from a clinical psychologist throughout the 6-month study period to address any distress that may arise.

We think it is essential that we provide participants with comprehensive psychoeducation to understand and manage the effects of the medication before they enroll, especially to prepare them for the conclusion of the study.

However, if the public’s excitement around GLP-1 medications gets ahead of the science, potentially dangerous scenarios could appear in which a growing number of people with binge eating disorder begin taking them for off-label use.

All the more reason to understand how these drugs impact the brain and to establish an informed foundation for the development of targeted and effective treatments for the world’s most common eating disorder.